Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various factors in the kallikrein-kinin system were evaluated in acute and chronic pancreatitis. It was noted in particular that plasma trypsin and glandular kallikrein increased markedly in acute phase of pancreatitis and its correlation with amylase was observed. Plasma prekallikrein (PPK) decreased in acute pancreatitis, but increased in chronic pancreatitis. A negative correlation was noted between PPK and kallikrein like activity. Both HMW and LMW kininogen decreased in acute pancreatitis. It was presumed from these findings that the increase in kinin and its activation at the acute phase of pancreatitis might be due to kallikrein or trypsin originating from the pancreas.
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PMID:Role of the kallikrein-kinin system in human pancreatitis. 248 54

We have developed a sensitive and specific radioimmunoassay which allows the detection of human glandular kallikrein in biologic fluids at a level of 40 pg/ml. The antisera did not recognize human plasma kallikrein and glandular kallikrein from other species including marmoset. Furthermore the antibody did not bind pro-kallikrein but was specific for the trypsin activated kallikrein. The antibody inhibited the kininogenase activity of standard kallikrein incubated with human kininogen. However active kallikrein inhibited by inhibitors bound at the active site is still detectable, indicating that the antibody is specific for the structure of the active form but not for the active site. In normotensive subjects, daily urinary kallikrein excretion increased with age until 30, then a decrease was observed. In renal transplanted recipients a progressive increase of the active form was found. A low concentration of immunoreactive active kallikrein was detected in lymphatic fluids of patients suffering from acute pancreatitis treated by lymphatic drainage; although this kallikrein is the active immunoreactive form, a very weak kininogenase activity was measured, suggesting a partial inhibition by anti-proteases. These data provide complementary evidence for the physiological and pathological role of glandular kallikrein.
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PMID:Direct radioimmunoassay of active and inactive human glandular kallikrein: some physiological and pathological variabilities. 266 24

Glandular kallikrein in human plasma was partially purified by immunoaffinity column (1.0 X 2.0 cm) and was measured by a radioimmunoassay (RIA). Plasma (5-10 ml) was diluted with an equal volume of 10 mmol/l sodium phosphate buffer, pH 7.4, containing 0.9% NaCl (PBS) and was applied to an immunoaffinity column from which glandular kallikrein was eluted with 3 mol/l NaSCN (20 ml). The enzymic fraction was concentrated with an Amicon PM 10 filter and dialyzed against PBS. The final recovery of the enzyme was 51.6 +/- 1.6% (mean +/- SD), determined by using [125I]kallikrein. The usable range of the standard curve covered 2.5-100 ng/tube. The coefficient of variation within the series was 5.9%, and the coefficient of variation between the series was 7.6%. In healthy controls (n = 25), the plasma content of glandular kallikrein was 1.36 +/- 0.39 ng/ml. In patients with acute pancreatitis (n = 6), the plasma concentration was 8.02 +/- 6.15 ng/ml, significantly different from the control group (p less than 0.01).
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PMID:Radioimmunoassay of glandular kallikrein in human plasma after partial purification by immunoaffinity column. 355 28